Gut Dysbiosis Causes Inflammatory Bowel Disease
Inflammatory Bowel Disease (IBD) is a clinical term for Crohn's disease and ulcerative colitis, both of which are chronic intestinal inflammatory pathologies with periods of remission and activity.
The intestinal microbiota is an important player in normal human gut physiology, with direct involvement in gut integrity and neurotransmission regulation, and it influences the outcome of IDB inflammatory processes.
Many factors, including smoking, sugary diets, drug exposure, and oral contraceptives, are responsible for gut dysbiosis are also responsible for IBD.
The gut microbiota is mostly bacteria along with fungal, and viral composition in the gastrointestinal (GI) tract under non-pathological conditions, which plays a critical role in the regulation of neurotransmission.
These non-pathogenic micro-organisms maintain the gut epithelial integrity, maturation and modulation of the immune system, and degradation of metabolites such as carbon, polysaccharides, and short-chain fatty acids (SCFAs).
Under normal gut conditions, there are more good bacteria have been found; meanwhile, more harmful bacteria have been found under pathological intestine conditions. This pathological bacterial overgrowth is better known as intestinal dysbiosis.
The intestinal epithelial barrier, along with the intestinal microbiota, is regarded as an essential functional unit in GI physiology and pathophysiology.
An alteration in the structure of the intestinal barrier can lead to an altered immune response and intestinal dysbiosis as part of the events that contribute to the pathogenesis of IBD.
Increased paracellular permeability has been observed in nearly 40% of Crohn's disease patients with a previously established diagnosis of IBD.
The central nervous system (CNS) and the gastrointestinal tract (GI tract) communicate via a bidirectional system known as the gut-brain axis (GBA), which includes serotonin as a key neurotransmitter.
GBA is a complex network of biochemical signaling that involves the CNS and enteric nervous system (ENS), with the ability to execute and regulate normal gut functioning as well as cognitive and neurodegenerative disorders due to the microbiota's ability to produce neurotransmitters and neuromodulators like tryptophan and glutamine.
There is a chance that these neuromodulators will develop abnormalities in the presence of intestinal dysbiosis.
Under pathological conditions and abnormal GBA and hypothalamic–pituitary–adrenal axis (HPA) signaling, patients may present increased levels of serotonin, thus favoring different illnesses, especially inflammatory gut processes such as IBD.
The dietary composition has also been considered a risk factor, as it can disrupt the normal gut microbiota, especially when foods such as sodas, chocolate, and artificial sweeteners are included.
Intestinal permeability has been found to be increased in mice fed a high-sugar diet. Besides the influence of diet, increased serum LPS levels and decreased microbiota diversity can lead to reduced production of SCFAs.
Crohn’s disease is characterized by transmural damage. Patients may present with perianal pain, bleeding, incontinence, fistulization, abscesses, and hemorrhoidal illness.
Crohn’s disease can also be characterized by the presence of extraintestinal manifestations, the most common being enthesitis and axial or peripheric arthritis.
On the other hand, ulcerative colitis can produce chronic inflammation of the colonic mucosa, leading to manifestations such as proctitis, bloody stools, abdominal pain, fatigue, fecal incontinence, arthralgias, and erythema nodosum.
In both ulcerative colitis and Crohn’s disease, the CNS is involved, specifically leading to psychological or psychiatric manifestations.
It has been observed that between 15% and 25% of patients with IBD developed depression, while 30% presented with anxiety.
Furthermore, it may be accompanied by sleep difficulties and fatigue. As part of the neurological involvement in patients with IBD, deficits in attention and executive function in adults have been observed.
Controlling and avoiding Crohn's disease and ulcerative colitis requires a healthy gut microbiota.